Publications
1996
Arts E J, Stetor S R, Li X, Rausch J W, Howard K J, Ehresmann B, North T W, Wohrl B M, Goody R S, Wainberg M A, Grice S F
Dans: Proc Natl Acad Sci U S A, vol. 93, no. 19, p. 10063-10068, 1996, ISBN: 8816751, (0027-8424 Journal Article).
Résumé | Liens | BibTeX | Étiquettes: Amino Acyl/chemistry/*metabolism RNA, Animals Base Sequence Cats DNA, Equine/genetics/*metabolism Kinetics Molecular Sequence Data Nucleic Acid Conformation RNA, Genetic, Non-U.S. Gov't Support, P.H.S. Templates, Transfer, U.S. Gov't, Unité ARN, Viral HIV-1/genetics/*metabolism Horses Human Infectious Anemia Virus, Viral/*biosynthesis Genome, Viral/chemistry/*metabolism RNA-Directed DNA Polymerase/*metabolism SIV/genetics/*metabolism Support
@article{,
title = {Initiation of (-) strand DNA synthesis from tRNA(3Lys) on lentiviral RNAs: implications of specific HIV-1 RNA-tRNA(3Lys) interactions inhibiting primer utilization by retroviral reverse transcriptases},
author = {E J Arts and S R Stetor and X Li and J W Rausch and K J Howard and B Ehresmann and T W North and B M Wohrl and R S Goody and M A Wainberg and S F Grice},
url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8816751},
isbn = {8816751},
year = {1996},
date = {1996-01-01},
journal = {Proc Natl Acad Sci U S A},
volume = {93},
number = {19},
pages = {10063-10068},
abstract = {Initiation of minus (-) strand DNA synthesis was examined on templates containing R, U5, and primer-binding site regions of the human immunodeficiency virus type 1 (HIV-1), feline immunodeficiency virus (FIV), and equine infectious anemia virus (EIAV) genomic RNA. DNA synthesis was initiated from (i) an oligoribonucleotide complementary to the primer-binding sites, (ii) synthetic tRNA(3Lys), and (iii) natural tRNA(3Lys), by the reverse transcriptases of HIV-1, FIV, EIAV, simian immunodeficiency virus, HIV type 2 (HIV-2), Moloney murine leukemia virus, and avian myeloblastosis virus. All enzymes used an oligonucleotide on wild-type HIV-1 RNA, whereas only a limited number initiated (-) strand DNA synthesis from either tRNA(3Lys). In contrast, all enzymes supported efficient tRNA(3Lys)-primed (-) strand DNA synthesis on the genomes of FIV and EIAV. This may be in part attributable to the observation that the U5-inverted repeat stem-loop of the EIAV and FIV genomes lacks an A-rich loop shown with HIV-1 to interact with the U-rich tRNA anticodon loop. Deletion of this loop in HIV-1 RNA, or disrupting a critical loop-loop complex by tRNA(3Lys) extended by 9 nt, restored synthesis of HIV-1 (-) strand DNA from primer tRNA(3Lys) by all enzymes. Thus, divergent evolution of lentiviruses may have resulted in different mechanisms to use the same host tRNA for initiation of reverse transcription.},
note = {0027-8424
Journal Article},
keywords = {Amino Acyl/chemistry/*metabolism RNA, Animals Base Sequence Cats DNA, Equine/genetics/*metabolism Kinetics Molecular Sequence Data Nucleic Acid Conformation RNA, Genetic, Non-U.S. Gov't Support, P.H.S. Templates, Transfer, U.S. Gov't, Unité ARN, Viral HIV-1/genetics/*metabolism Horses Human Infectious Anemia Virus, Viral/*biosynthesis Genome, Viral/chemistry/*metabolism RNA-Directed DNA Polymerase/*metabolism SIV/genetics/*metabolism Support},
pubstate = {published},
tppubtype = {article}
}
Initiation of minus (-) strand DNA synthesis was examined on templates containing R, U5, and primer-binding site regions of the human immunodeficiency virus type 1 (HIV-1), feline immunodeficiency virus (FIV), and equine infectious anemia virus (EIAV) genomic RNA. DNA synthesis was initiated from (i) an oligoribonucleotide complementary to the primer-binding sites, (ii) synthetic tRNA(3Lys), and (iii) natural tRNA(3Lys), by the reverse transcriptases of HIV-1, FIV, EIAV, simian immunodeficiency virus, HIV type 2 (HIV-2), Moloney murine leukemia virus, and avian myeloblastosis virus. All enzymes used an oligonucleotide on wild-type HIV-1 RNA, whereas only a limited number initiated (-) strand DNA synthesis from either tRNA(3Lys). In contrast, all enzymes supported efficient tRNA(3Lys)-primed (-) strand DNA synthesis on the genomes of FIV and EIAV. This may be in part attributable to the observation that the U5-inverted repeat stem-loop of the EIAV and FIV genomes lacks an A-rich loop shown with HIV-1 to interact with the U-rich tRNA anticodon loop. Deletion of this loop in HIV-1 RNA, or disrupting a critical loop-loop complex by tRNA(3Lys) extended by 9 nt, restored synthesis of HIV-1 (-) strand DNA from primer tRNA(3Lys) by all enzymes. Thus, divergent evolution of lentiviruses may have resulted in different mechanisms to use the same host tRNA for initiation of reverse transcription.